Novel Shank3 mutant exhibits behaviors with face validity for autism and altered striatal and hippocampal function
Open accessAbstract
Mutations/deletions in the SHANK3 gene are associated with autism spectrum disorders and intellectual disability. Here, we present electrophysiological and behavioral consequences in novel heterozygous and homozygous mice with a transcriptional stop cassette inserted upstream of the PDZ domain‐coding exons in Shank3 (Shank3 E13 ). Insertion of a transcriptional stop cassette prior to exon 13 leads to loss of the two higher molecular weight isoforms of Shank3. Behaviorally, both Shank3 E13 heterozygous (HET) and homozygous knockout (KO) mice display increased repetitive grooming, deficits in social interaction tasks, and decreased rearing. Shank3 E13 KO mice also display deficits in spatial memory in the Morris water maze task. Baseline hippocampal synaptic transmission and short‐term plasticity are preserved in Shank3 E13 HET and KO mice, while both HET and KO mice exhibit impaired hippocampal long‐term plasticity. Additionally, Shank3 E13 HET and KO mice display impaired striatal glutamatergic synaptic transmission. These results demonstrate for the first time in this novel Shank3 mutant that both homozygous and heterozygous mutation of Shank3 lead to behavioral abnormalities with face validity for autism along with widespread synaptic dysfunction. Autism Res 2017, 10: 42–65 . © 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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Consistent with prior reports, HET mice generally do not display anxiety-related behavior.
“Therefore, consistent with prior reports 22,33, the HET mice generally do not display anxiety-related behavior.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [33]
The HET mice therefore displayed diminished sociability.
“The HET mice therefore displayed diminished sociability 22,33.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [33]
Heterozygous constructs were used to mimic the physiological expression of Shank3 and because, unlike animals with homozygous mutations, they generally do not exhibit motoric dysfunction, anxiety or self-injurious behavior that could potentially confound social testing.
“In our study, we used heterozygous constructs to mimic the physiological expression of Shank3 and because, unlike animals with homozygous mutations, they generally do not exhibit motoric dysfunction, anxiety or self-injurious behavior that could potentially confound social testing 22,33.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [33]
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- Jaramillo TC Speed HE Xuan Z Reimers JM Liu S Powell CM Altered striatal synaptic function and abnormal behaviour in Shank3 exon4–9 deletion mouse model of autism Autism Research 2016 9 350 375 26559786 PMC4857590
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Self-citation
- Authors
- Jaramillo, T. C., Speed, H. E., Xuan, Z., Reimers, J. M., Escamilla, C. O., Weaver, T. P., Liu, S., Filonova, I., & Powell, C. M.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Powell, Craig M.
- Venue
- Autism Research
- Publisher
- Wiley
- Published
- 2016-08-05
- Volume
- 10
- Issue
- 1
- Pages
- 42-65
- ISSN
- 1939-3792 (ISSN-L)
- 1939-3806
- PMC
- PMC5274551
- OpenAlex
- W2497572150
- Cited by
- 119
- References
- 61
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 14 · 2023: 14 · 2022: 12 · 2021: 18 · 2020: 9 · 2019: 11 · 2018: 13 · 2017: 7
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Autism Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Child Health and Human Development (R01HD069560, R21HD065290, R01HD069560‐S1)
- Autism Science Foundation
- Hartwell Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- SHANK3, autism spectrum disorder, intellectual disability, PDZ domain, heterozygous knockout mice, social interaction deficits, rearing behavior, spatial memory, synaptic dysfunction
- MeSH terms
- Animals, Autistic Disorder, Behavior, Animal, Corpus Striatum, Disease Models, Animal, Exons, Female, Hippocampus, Male, Microfilament Proteins, Mutation, Nerve Tissue Proteins, Synaptic Transmission, Blotting, Western, Reproducibility of Results, Sequence Deletion, Mice, Knockout, Mice
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